Cancer Patient Lab: Community for Cancer Patients Seeking Personalized Treatment

“Launch Meeting: Introductions and Purpose” (Brian McCloskey, Rick Stanton, Brad Power) [#1] March 23, 2022 Brad Power “My hope is to help Brian, myself, and patients to come to decide what the next best therapy is after the standard of care as we push into immunotherapies and combinations of conventional, targeted, and immunotherapies.

” – Rick Stanton “My objective is to determine what is going to be the next best therapy for me. “ – Brian McCloskey Meeting Summary Advanced prostate cancer patients Brian McCloskey and Rick Stanton introduced themselves, their medical history, and their objectives for the Prostate Cancer Lab. ●Brian McCloskey: 56-year-old tech marketing executive; diagnosed 5.

5 years ago; on abiraterone; sees the challenge of personalizing his treatment as hinging on data and analytics; wants to bring cutting edge diagnostic data and integrate it to understand his disease and guide his treatment. ●Rick Stanton: bioinformatician with many years in the pharmaceutical industry, including at Human Longevity, Inc.

, and Amgen; Stage IV; on chemo; wants to bring emerging research diagnostic technologies to his treatment decisions. CancerHacker Lab founder Brad Power moderated and shared an overview of the Cancer Patient Lab and its purpose. ●Building on the hackathon for advanced prostate cancer patient Bryce Olson in 2021.

●Lab process: attract patients, gather data, analyze data and find treatment options, define treatment strategy. ●Have attracted diverse companies and individuals willing to help: diagnosticians, bioinformaticians, treatment matching, patient advocates, and clinicians.

●Focus on accelerating the use of cutting edge diagnostics (RNA, proteomics, single cell, spatial analysis), which are currently “Research Use Only”, for clinical decision-making.

Several of the participants introduced themselves, including: ●Nik Schork: of TGen, an organization bridging between health data and clinical guidance - has developed a protocol, approved by an IRB, to grant patients access to research data about them. ●Rick Davis: leader of AnCan, a community of cancer patients - clarified treatment options.

●Lea Ann Biafora: oncology nurse, founder of Beacon Associates; Jason Sager: pediatric oncologist; Stacy Hurt: patient advocate, colorectal cancer survivor; Jeff Waldron: healthcare community connector; Jan Sobieralski: advanced prostate cancer patient.

“Launch Meeting: Introductions and Purpose” (Brian McCloskey, Rick Stanton, Brad Power) [#1] The information and opinions expressed on this website or platform, or during discussions and presentations (both verbal and written) are not intended as health care recommendations or medical advice by Cancer Patient Lab/Prostate Cancer Lab, its principals, presenters, participants, or representatives for any medical treatment, product, or course of action.

tions or medical advice by Cancer Patient Lab/Prostate Cancer Lab, its principals, presenters, participants, or representatives for any medical treatment, product, or course of action. You should always consult a doctor about your specific situation before pursuing any health care program, treatment, product or other course of action that might affect your health.

“Launch Meeting: Introductions and Purpose” (Brian McCloskey, Rick Stanton, Brad Power) [#1] Meeting Notes Brian McCloskey: I’m a 56-year-old father of three and husband. I was diagnosed five-and-a- half years ago. I have been on an interesting journey since.

Professionally, I spent the better part of 25 years building personalized consumer experiences in e-commerce and high tech, and most recently managed marketing for the largest healthcare staffing firm in the country, AMN Healthcare. My background is very data and digitally oriented.

When I was diagnosed with cancer I realized there were some opportunities in how we used data to better personalize the experience, and hoped to use my background in approaching my cancer. The essence is trying to understand my cancer before we move onto treating it. It’s the same as when we used lots of data to personalize consumer experiences.

I haven’t seen anything that tells me that that analogy doesn’t hold in medicine. There’s a long way to go in medicine, and that is what this is about. How do we use data to more intelligently treat us? My passion is surfing. I live in San Diego. I passed it onto my kids. Rick Stanton: I’m a surfer as well, though not as good as Brian. I have two kids and a wonderful wife.

My daughter moved to Hawaii to surf. I’m Stage IV. I’m on chemo. I have gone through multiple rounds. My prostate cancer was discovered after noting a jump in my PSA at a yearly checkup. I had no symptoms. It turns out I have a CDK12 mutation, which is aggressive, but opens up some therapy options. My goal is like Brian’s.

There are about 1,000 clinical trials going on for advanced prostate cancer. They are targeting roughly 25 or 30 molecular targets of the immune system or in the cancer cell. I and Brian are at or nearing the end of the standard of care for NCCN guidelines. The standard of care includes androgen (hormone) blocking drugs, and then you go on chemo.

I am on my fifth round of chemo and need to know what to do when it fails. You can’t stay on chemo forever. I’m having tingling in my fingers. My hope is to help Brian, myself, and patients to come to decide what the next best therapy is after the standard of care as we push into immunotherapies and combinations of conventional, targeted, and immunotherapies.

I have 3 or 4 doctors, so I am getting multiple counsel. Different doctors have different clinical trial options. I’m finding that none of these treatment options are defined by my state. RNA seq is typically not used. Mutations are used, e.g., my CDK12 mutation is being used to guide my therapy.

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ard of care as we push into immunotherapies and combinations of conventional, targeted, and immunotherapies. I have 3 or 4 doctors, so I am getting multiple counsel. Different doctors have different clinical trial options. I’m finding that none of these treatment options are defined by my state. RNA seq is typically not used. Mutations are used, e.g., my CDK12 mutation is being used to guide my therapy.

“Launch Meeting: Introductions and Purpose” (Brian McCloskey, Rick Stanton, Brad Power) [#1] Tumor mutational burden is used and some basics. I’m hoping to get guidance on which trial or therapy to try next, to either manage my disease well or find a cure. Brad Power: Any more details on your medical history? How has your PSA responded to different treatments?

Rick Stanton: I was diagnosed in late 2019. My treatments have been salvage radiation, Lupron, and Casodex, which controlled my PSA for 13 months. Then I went on darolutamide, which is a next-generation androgen receptor blocker. That didn’t do so much. I was on that for 4 months, and my PSA started rising to 3.6. My doubling time was about a month. It was not being controlled.

It was determined I should go on docetaxel chemo, which I have been on since December. It brought me from 3.6 to 2.6, so only a marginal drop in my PSA. I have a nodal disease. I have 5 or 6 lymph nodes that have cancer in them, from my neck to my pelvis, as shown in a combination of CT and PSMA scans. I’m currently at a PSA of 2.6.

My largest lymph node is about a centimeter, in the middle of my chest. I requested IHC stains from my primary tumor, which might guide my TILs and predict responsiveness to my tumor. Brad: You might have noticed implicitly that Rick is a bioinformatician by background.

Brian McCloskey: Here is a graphic that describes my journey of treatments and responses: Exhibit 1: Biomarker/Treatment Overlay - 8 Key Decisions I was diagnosed in 2016. I had a radical prostatectomy. My DNA mutations are in the blue box: TP53, PBRM1, and TMPRSS2-ERG.

I went on a number of different treatments: hormone therapy, radiation, a second line hormone therapy with apalutamide (decision number 4). Then I went on a holiday, and as soon as I went on a holiday, my disease came roaring back. My Gleason is a 4.

“Launch Meeting: Introductions and Purpose” (Brian McCloskey, Rick Stanton, Brad Power) [#1] disease. I have 6 metastatic lesions in my peretenium. That was discovered in July of 2020. I had robotic surgery in August of 2020. We determined that my DNA mutations were the same as from my primary tumor in 2016. Rick did an amazing job of quarterbacking an RNA seq analysis with Tempus.

There were a lot of findings from that; of note: expressions of CD276, CD357, TD02, and FOLH1 (PSMA). TILS 0%. Definitely some challenges in terms of a very immunosuppressive environment.

have 3 or 4 doctors, so I am getting multiple counsel. Different doctors have different clinical trial options. I’m finding that none of these treatment options are defined by my state. RNA seq is typically not used. Mutations are used, e.g., my CDK12 mutation is being used to guide my therapy.

“Launch Meeting: Introductions and Purpose” (Brian McCloskey, Rick Stanton, Brad Power) [#1] Tumor mutational burden is used and some basics. I’m hoping to get guidance on which trial or therapy to try next, to either manage my disease well or find a cure. Brad Power: Any more details on your medical history? How has your PSA responded to different treatments?

Rick Stanton: I was diagnosed in late 2019. My treatments have been salvage radiation, Lupron, and Casodex, which controlled my PSA for 13 months. Then I went on darolutamide, which is a next-generation androgen receptor blocker. That didn’t do so much. I was on that for 4 months, and my PSA started rising to 3.6. My doubling time was about a month. It was not being controlled.

It was determined I should go on docetaxel chemo, which I have been on since December. It brought me from 3.6 to 2.6, so only a marginal drop in my PSA. I have a nodal disease. I have 5 or 6 lymph nodes that have cancer in them, from my neck to my pelvis, as shown in a combination of CT and PSMA scans. I’m currently at a PSA of 2.6.

My largest lymph node is about a centimeter, in the middle of my chest. I requested IHC stains from my primary tumor, which might guide my TILs and predict responsiveness to my tumor. Brad: You might have noticed implicitly that Rick is a bioinformatician by background.

Brian McCloskey: Here is a graphic that describes my journey of treatments and responses: Exhibit 1: Biomarker/Treatment Overlay - 8 Key Decisions I was diagnosed in 2016. I had a radical prostatectomy. My DNA mutations are in the blue box: TP53, PBRM1, and TMPRSS2-ERG.

I went on a number of different treatments: hormone therapy, radiation, a second line hormone therapy with apalutamide (decision number 4). Then I went on a holiday, and as soon as I went on a holiday, my disease came roaring back. My Gleason is a 4.

“Launch Meeting: Introductions and Purpose” (Brian McCloskey, Rick Stanton, Brad Power) [#1] disease. I have 6 metastatic lesions in my peretenium. That was discovered in July of 2020. I had robotic surgery in August of 2020. We determined that my DNA mutations were the same as from my primary tumor in 2016. Rick did an amazing job of quarterbacking an RNA seq analysis with Tempus.

There were a lot of findings from that; of note: expressions of CD276, CD357, TD02, and FOLH1 (PSMA). TILS 0%. Definitely some challenges in terms of a very immunosuppressive environment. After my surgery, since we knew we didn’t get it all, I started on systemic therapy with chemo and pembrolizumab (Keytruda) in October 2020.

; of note: expressions of CD276, CD357, TD02, and FOLH1 (PSMA). TILS 0%. Definitely some challenges in terms of a very immunosuppressive environment. After my surgery, since we knew we didn’t get it all, I started on systemic therapy with chemo and pembrolizumab (Keytruda) in October 2020. 6 rounds. Then I remained on pembro until October 2021. Then my PSA began to rise and lesions re-appeared.

I had “no evidence of disease” shortly after my surgery. I started abiraterone in November of 2021. My PSA was at .91, and it has dropped to a .45. I am currently responsive to abi, which is great. But I don’t know how much mileage I’m going to get on this. I know that the likelihood of becoming hormone-insensitive is high.

My objective is to determine what is going to be the next best therapy for me. Here is a quick snapshot of my journey in terms of the sheer number of medical visits: Exhibit 2: 205 Cancer Visits over 5.

“Launch Meeting: Introductions and Purpose” (Brian McCloskey, Rick Stanton, Brad Power) [#1] Imaging – 10% Here is my table of treatment options: Exhibit 3 - Treatment options I want to get much smarter about which treatments I can rule out, and which treatments are going to be most relevant for me. Today the way that decisions are made is largely based on the stage of the disease (e.g.

, metastatic), hormone-sensitive or not hormone-sensitive, and the medical history and relate that to clinical trials and mass treatment response rates. I believe we can do better than that. We found some interesting insights from my DNA analysis. We had some interesting results from the RNA seq analysis.

I wonder what else we can find if we continue to look from a genomic perspective, from a cell perspective, an extracellular perspective; look at my immune system, and maybe other factors, and help me do a better job to rule out treatments and prioritize those that will provide the greatest response. My mission is to live as long as I can.

Exhibit 4 - My mission is to live my best life, as long as I can.

“Launch Meeting: Introductions and Purpose” (Brian McCloskey, Rick Stanton, Brad Power) [#1] I am grateful for the amazing care I’ve had, and the advancements and the support I have received. I also see there is a chance to accelerate the pace of translational medicine. I’m thankful to have Rick and Brad on this journey.

I believe we are trying to better use the insights that exist in the lab and bring them to treat our diseases more effectively. I have conversations every day with so many amazing doctors, scientists, and researchers about how those improvements are happening. I want us to take a different approach. This prostate cancer lab represents an opportunity to take a unique approach to do that.

Jan Sobieralski: I want to compliment Brian on his flowchart. This could help in any diagnosis. It’s a great way to present your case.

“Laun